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首页|期刊导航|中国临床药理学与治疗学|蛇床子素调节PI3K/Akt/mTOR信号通路对老龄自发性高血压大鼠肾氧化应激损伤的影响

蛇床子素调节PI3K/Akt/mTOR信号通路对老龄自发性高血压大鼠肾氧化应激损伤的影响OA北大核心CSTPCD

Effects of osthole on renal oxidative stress injury in aged spontane-ously hypertensive rats by regulating PI3K/Akt/mTOR signaling path-way

中文摘要英文摘要

目的:探究蛇床子素对老龄自发性高血压大鼠的影响机制.方法:购买20月龄的老龄自发性高血压大鼠(SHRs)及健康Wistar-Kyoto(WKY)大鼠,对SHRs进行蛇床子素灌胃治疗处理持续8周.对大鼠收缩压及舒张压进行监测,使用苏木精-伊红(H&E)、碘酸雪夫染色(PAS)和Masson染色观察大鼠肾脏组织病理学变化.使用ELISA试剂盒检测大鼠肾脏超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽(GSH)活性.采用Western blot对PI3K/Akt/mTOR信号通路相关蛋白进行检测.结果:蛇床子素降低SHRs收缩压及舒张压,改善了 SHRs大鼠肾脏的组织病理学变化,降低SHRs肾脏MDA活性,提升SOD及GSH活性.蛇床子素降低p-Pl3K、p-Akt、p-mTOR水平.结论:蛇床子素通过降低PI3K/Akt/mTOR信号通路活性发挥对老龄自发性高血压大鼠肾氧化应激损伤的保护作用.

AIM:To explore the mechanism of ost-hole on elderly spontaneously hypertensive rats.METHODS:20-month-old spontaneously hyperten-sive rats(SHRs)and healthy Wistar-Kyoto(WKY)rats were purchased.SHRs were treated with ost-hole(i.g.)for 8 weeks.The systolic blood pressure and diastolic blood pressure of rats were moni-tored.Hematoxylin-eosin staining(H&E),periodic acid-schiff staining(PAS)and Masson staining were used to observe the pathological changes of rat kid-ney tissues.The activity of superoxide dismutase(SOD),malondialdehyde(MDA)and glutathione(GSH)in rat kidney was detected by ELISA kit.PI3K/Akt/mTOR signaling pathway related proteins were detected by western blot.RESULTS:Osthole re-duced the systolic and diastolic blood pressure of SHRs,improved the histopathological changes of SHRs kidney,reduced the activity of MDA in SHRs kidney,and increased the activity of SOD and GSH.Osthole reduced the levels of p-PI3K,p-Akt and p-mTOR.CONCLUSION:Osthole reduces the activity of PI3K/Akt/mTOR signaling pathway and exerts a protective effect on renal oxidative stress injury in aged spontaneously hypertensive rats.

余丹;刘宗涛;严小宏;程京;李玲

武汉市红十字会医院,武汉 430022,湖北华中科技大学医院,武汉 430071,湖北

临床医学

自发性高血压老龄蛇床子素氧化应激PI3K/Akt/mTOR

spontaneous hypertensionagingos-tholeoxidative stresskidneyPI3K/Akt/mTOR

《中国临床药理学与治疗学》 2024 (003)

277-282 / 6

10.12092/j.issn.1009-2501.2024.03.005

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